National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing, China.
National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing, China; China Animal Husbandry Industry Co. Ltd, Beijing, China.
Vet Microbiol. 2024 Nov;298:110243. doi: 10.1016/j.vetmic.2024.110243. Epub 2024 Aug 30.
Classical swine fever virus (CSFV) and porcine productive and respiratory syndrome virus (PRRSV) both are significant infectious pathogens in pigs and pose great threats to the healthy development of the pig industry. PRRSV infection often reduces the antibody level of the CSFV attenuated vaccine and even leads to immune failure. In order to elucidate the potential mechanism of CSFV proliferation inhibition by PRRSV and screen out drugs that enhance the vaccine immune effect, we conducted experiments in the PAM39 cell line that can simultaneously support both PRRSV and CSFV infection. The results showed that PRRSV infection could induce gasdermin D (GSDMD) cleavage, promote cell pyroptosis, increase IL-1β secretion, and then inhibit CSFV replication. However, Astragalus polysaccharide treatment could reverse this phenomenon. The results elucidate the molecular mechanism of CSFV vaccine immune failure caused by PRRSV co-infection from the perspective of pyroptosis and provide a scientific basis for the prevention and control of clinical co-infection diseases.
古典猪瘟病毒（CSFV）和猪繁殖与呼吸综合征病毒（PRRSV）都是猪的重要传染性病原体，对猪业的健康发展构成了巨大威胁。PRRSV 感染通常会降低 CSFV 减毒疫苗的抗体水平，甚至导致免疫失败。为了阐明 PRRSV 抑制 CSFV 增殖的潜在机制并筛选出增强疫苗免疫效果的药物，我们在能够同时支持 PRRSV 和 CSFV 感染的 PAM39 细胞系中进行了实验。结果表明，PRRSV 感染可诱导 Gasdermin D（GSDMD）裂解，促进细胞焦亡，增加 IL-1β 分泌，从而抑制 CSFV 复制。然而，黄芪多糖处理可逆转这种现象。该结果从焦亡的角度阐明了 PRRSV 共感染导致 CSFV 疫苗免疫失败的分子机制，为临床共感染疾病的防控提供了科学依据。
